Lund L R, Rømer J, Thomasset N, Solberg H, Pyke C, Bissell M J, Danø K, Werb Z
Laboratory of Radiobiology and Environmental Health, University of California, San Francisco 94143-0750, USA.
Development. 1996 Jan;122(1):181-93. doi: 10.1242/dev.122.1.181.
Postlactational involution of the mammary gland is characterized by two distinct physiological events: apoptosis of the secretory, epithelial cells undergoing programmed cell death, and proteolytic degradation of the mammary gland basement membrane. We examined the spatial and temporal patterns of apoptotic cells in relation to those of proteinases during involution of the BALB/c mouse mammary gland. Apoptosis was almost absent during lactation but became evident at day 2 of involution, when beta-casein gene expression was still high. Apoptotic cells were then seen at least up to day 8 of involution, when beta-casein gene expression was being extinguished. Expression of sulfated glycoprotein-2 (SGP-2), interleukin-1 beta converting enzyme (ICE) and tissue inhibitor of metalloproteinases-1 was upregulated at day 2, when apoptotic cells were seen initially. Expression of the matrix metalloproteinases gelatinase A and stromelysin-1 and the serine proteinase urokinase-type plasminogen activator, which was low during lactation, was strongly upregulated in parallel starting at day 4 after weaning, coinciding with start of the collapse of the lobulo-alveolar structures and the intensive tissue remodeling in involution. The major sites of mRNA synthesis for these proteinases were fibroblast-like cells in the periductal stroma and stromal cells surrounding the collapsed alveoli, suggesting that the degradative phase of involution is due to a specialized mesenchymal-epithelial interaction. To elucidate the functional role of these proteinases during involution, at the onset of weaning we treated mice systemically with the glucocorticoid hydrocortisone, which is known to inhibit mammary gland involution. Although the initial wave of apoptotic cells appeared in the lumina of the gland, the dramatic regression and tissue remodeling usually evident by day 5 was substantially inhibited by systemic treatment with hydrocortisone. mRNA and protein for gelatinase A, stromelysin-1 and uPA were weakly induced, if at all, in hydrocortisone-treated mice. Furthermore, mRNA for membrane-type matrix metalloproteinase decreased after hydrocortisone treatment and paralleled the almost complete inhibition of activation of latent gelatinase A. Concomitantly, the gland filled with an overabundance of milk. Our data support the hypothesis that there are at least two distinct phases of involution: an initial phase, characterized by induction of the apoptosis-associated genes SGP-2 and ICE and apoptosis of fully differentiated mammary epithelial cells without visible degradation of the extracellular matrix, and a second phase, characterized by extracellular matrix remodeling and altered mesenchymal-epithelial interactions, followed by apoptosis of cells that are losing differentiated functions.
经历程序性细胞死亡的分泌上皮细胞凋亡,以及乳腺基底膜的蛋白水解降解。我们研究了BALB/c小鼠乳腺退化过程中凋亡细胞与蛋白酶的空间和时间模式。哺乳期几乎没有凋亡现象,但在退化第2天变得明显,此时β-酪蛋白基因表达仍很高。然后至少在退化第8天可见凋亡细胞,此时β-酪蛋白基因表达正在消失。硫酸化糖蛋白-2(SGP-2)、白细胞介素-1β转换酶(ICE)和金属蛋白酶组织抑制剂-1在第2天上调表达,此时最初可见凋亡细胞。基质金属蛋白酶明胶酶A和基质溶解素-1以及丝氨酸蛋白酶尿激酶型纤溶酶原激活剂的表达在哺乳期很低,从断奶后第4天开始平行强烈上调,与小叶-腺泡结构开始塌陷和退化过程中强烈的组织重塑同时发生。这些蛋白酶的mRNA合成主要部位是导管周围基质中的成纤维细胞样细胞和塌陷肺泡周围的基质细胞,这表明退化的降解阶段是由于一种特殊的间充质-上皮相互作用。为了阐明这些蛋白酶在退化过程中的功能作用,在断奶开始时我们用已知可抑制乳腺退化的糖皮质激素氢化可的松对小鼠进行全身治疗。虽然最初一波凋亡细胞出现在腺腔中,但通常在第5天明显的显著退化和组织重塑被氢化可的松全身治疗显著抑制。在氢化可的松治疗的小鼠中,明胶酶A、基质溶解素-1和尿激酶型纤溶酶原激活剂的mRNA和蛋白即使有诱导也很微弱。此外,膜型基质金属蛋白酶的mRNA在氢化可的松治疗后减少,并与潜伏性明胶酶A激活的几乎完全抑制平行。同时,腺内充满了过多的乳汁。我们的数据支持这样的假说,即退化至少有两个不同阶段:初始阶段,其特征是凋亡相关基因SGP-2和ICE的诱导以及完全分化的乳腺上皮细胞凋亡,而细胞外基质无明显降解;第二阶段,其特征是细胞外基质重塑和间充质-上皮相互作用改变,随后是失去分化功能的细胞凋亡。